Term
|
Definition
| very specific (Ex. In order to become activated, T cells have to bind to foreign antigen that is presented on a self-MHC molecule |
|
|
Term
|
Definition
| T cell have to bind to foreign entigen that is presented on a self-MHC molecule |
|
|
Term
| MHC molecule presentation |
|
Definition
| can only present one molecule at a time, but it is capable of presenting many different peptides. |
|
|
Term
| Why do self-cells constantly display self-antigen on their MHC? |
|
Definition
| To survey for autoimmune T cells (those that react to self). If the T cell responds, it will be killed by apoptosis. |
|
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Term
|
Definition
| APCs engulf microbes, digest them in phagolysosomes, and retain the immunogenic peptides. After CLIP removal, these peptides are placed on MHC class II molecules and transported to the APC cell surface. The APC travels through the lymphatic system to a secondary lymph node, and the (now mature) APC interacts with Th0 cells by binding their class II MHC (displaying the antigen) to the Th0’s TCR |
|
|
Term
| Which cells use MHC class II |
|
Definition
|
|
Term
| Which cells use MHC class I |
|
Definition
| all nucleated cells use MHC I |
|
|
Term
| Which cells can interact with MHC II |
|
Definition
|
|
Term
| Which cells can bind to MHC I |
|
Definition
|
|
Term
|
Definition
| further stabilize the interaction between CD and MHC, and provide a more complete activation of Th0 (Ex. CD3, B7/CD28, etc) |
|
|
Term
| Why do Th0 differentiate into Th1 cells |
|
Definition
| for cell-mediated response against intracellular pathogens |
|
|
Term
| Why do Th0 differentiate into Th2 cells |
|
Definition
| for humoral immune-mediated response against extracellular pathogens |
|
|
Term
| Th2 secretes cytokines to: |
|
Definition
| upregulate B cells to become plasma cells and make antibodies |
|
|
Term
| Th1 secretes cytokines to: |
|
Definition
| upregulate cytotoxic T cells. Then Upregulated Tc cells use their TCR to seek out cells displaying that same antigen, displayed on class I MHC |
|
|
Term
| what happens to proteins from infected cells? |
|
Definition
| Proteins from infected cells are fragmented by proteolytic enzymes in cytosol to 8 or 9 amino acid peptides. Then they are transported across the ER membrane by TAPs, put on class I MHC, and transported to the cell surface. CD8 T cells then bind the class I MHC/antigen complex and kill the cell |
|
|
Term
| describe the genes encoding MHC |
|
Definition
| The genes encoding MHC (aka, the HLA/human leukocyte antigen) are the most polymorphic genes in our genome - so each person has different MHC genes so that our immune systems can tell self-MHC from foreign MHC. This is why organ transplants are rejected without immunosuppression. |
|
|
Term
|
Definition
| MHC also has co-dominant expression which means that both parental alleles of each MHC are expressed. |
|
|
Term
| what molecules display cytosolic antigens from nucleated cells? |
|
Definition
|
|
Term
|
Definition
| TCRs only recognize peptide antigens and are very specific to one exact antigen – this is because of schooling, gene rearrangement of VDJ segments in the thymus |
|
|
Term
| what conformation do most TCRs have? |
|
Definition
|
|
Term
| Where are gamma-delta TCRs found and why? |
|
Definition
| epithelial surfaces to recognize lipid antigens and damaged cells |
|
|
Term
| Can NKT cells recognize lipid antigens without gamma-delta TCRs? |
|
Definition
| NKT cells have alpha-beta TCR but recognize lipid antigens on class I MHC. |
|
|
Term
|
Definition
| proteins, lipids, carbohydrates, and nucleic acids |
|
|
Term
|
Definition
| BCRs are glycoproteins made up of 2 identical light, and 2 identical heavy chains. The light chains are either kappa or gamma. Both the heavy and light chains have both variable and constant regions. |
|
|
Term
| Development of heavy chain |
|
Definition
| The heavy chain starts out as mu or delta (IgM or IgD) when the antibody is an immature BCR. After antigen exposure: hypermutation, affinity maturation, isotype switching – changes the constant region to IgG, IgA, IgE |
|
|
Term
|
Definition
| BCRs are immature forms of antibodies that are membrane bound to the developing B cell. The BCR is able to bind a variety of similarly shaped antigens; they become more specific about antigen binding as they hypermutate and mature in secondary lymphoid organs (in the germinal center of the follicle). Daughter cells that hypermutate to a conformation that more poorly fit the antigen undergo apoptosis. |
|
|
Term
| function of 2 regions of TCR/BCR |
|
Definition
| TCRs and BCRs have variable regions that bind antigen and constant regions that bind to host immune cells. |
|
|
Term
| How to fully activate the T cell or B cell |
|
Definition
| In order to fully activate the T or B cell you need: 1) antigen/receptor binding and cross-linking between 2 receptors and 2) co-receptor binding – this activates signaling cascades |
|
|
Term
|
Definition
| Antigen receptors have VDJ regions that are spliced together (RAG), then are recombined for optimal antigen specificity |
|
|
Term
|
Definition
| During its time in the thymus, the T cell expresses: (1) CD2 – the adhesion molecule on T cells and NK cells (2) [Rearrange TCR genes] (3) CD25 (an IL-2 receptor) (4) CD3 (5) Both CD4 and CD8 (double positive) (6) If they can bind self-MHC class I, they become single positive CD8 (7) If they can bind self-MHC class II, they become single positive CD4 (8) If they can’t bind either MHC class, they die of apoptosis (9) The MHC molecules also present the T cell with self-antigen (10) If the T cell becomes activated to the self-antigen, it dies of apoptosis (11) 99% of T cell progenitors fail thymic schooling |
|
|
Term
| What do T cells do after leaving the Thymus |
|
Definition
| T cells circulate systemically after schooling in the thymus, in search of their antigens |
|
|
Term
|
Definition
| describes origin, growth (size change), and development (structural/shape change) |
|
|
Term
|
Definition
| NK cells (aka: large granular lymphocyte) is a type of cytotoxic lymphocyte that uses perforin and granzyme for cell killing. |
|
|
Term
| Characteristics of an NK cell |
|
Definition
| (1) Do not express TCR or CD3 (2) Do not have to be activated, but can be activated by IFNs and other cytokines (3) Can bind the Fc portion of antibodies to kill antibody-tagged cells (4) Secrete IFN and TNF to upregulate the immune response |
|
|
Term
| 3 components of adaptive immunity |
|
Definition
| (1) Antigen specific (2) Systemic (3) Memory |
|
|
Term
| Why shouldn't adaptive immunity respond to self-antigens? |
|
Definition
| Adaptive immunity should not respond to self-antigens (good to prevent autoimmunity, but bad in the case of organ transplantation, because the donated organ doesn’t have self-antigens and thus is attacked) |
|
|
Term
|
Definition
| peptides, nucleic acids, carbs, lipids, pollen grains, microorganisms |
|
|
Term
| Process of antigen capture, presentation, adaptive immune upregulation |
|
Definition
| (1) Antigens are captured by APCs in peripheral tissue (2) Antigens are processed to form MHC-peptide complexes (3) APCs mature and express molecules that will lead to binding and stimulation of T cells in secondary lymphoid organs (4) If the antigen has been bound by B cells, then both B and T cells cluster with APCs |
|
|
Term
| Major functions of T cells |
|
Definition
| Activate B cells (Th2); CMI (CD8); Suppression of the immune response (Tregs) |
|
|
Term
| Components of Immunological synapse |
|
Definition
| Antigen recognition by TCR on MHC; CD4/CD8 recognizes its appropriate MHC; Adhesion molecules (LFA-1/ICAM-1 or VLA-4/VCAM-1); Receptors for co-stimulation – CD40/CD40I, CD28/B7, CTLA-4/B7 for suppression; Cytokine receptors (IL-12, IL-2) |
|
|
Term
| Scenarios of proper or improper cell-cell interactions |
|
Definition
| (1) Healthy cells present self-antigen on MHC all the time too. In this way, selection against self-reactive T cells continues even outside of the thymus and bone marrow. (2) If a T cell binds to self-antigen on a healthy cell, that cell is eliminated. (3) If a T cell loosely binds to a self-antigen, but it is not a good fit (e.g., low affinity), nothing happens. (4) But if a T cell binds with high affinity to a foreign antigen, and the CD8 or CD4 binding to MHC is also good, then this successfully activates the immune system and there is an immune response. Now if that antigen is a self-antigen, and there is high affinity binding between the MHC and TCR as well as CD8 and MHC, then the immune response is against self, or autoimmune in nature. |
|
|
Term
|
Definition
| Th0 cell becomes Th1 with IFN and IL-12 activation. Th1 cells then produce IL-2, IFN, and TNF. |
|
|
Term
|
Definition
| Th0 cell becomes Th2 with IL-4 and IL-13 activation. Th2 cells then produce IL-4, 5, 6, and 10. |
|
|
Term
| What do CD8 T cells kill with |
|
Definition
| CD8 T cells kill using perforin (osmotic lysis) and granzymes/granulysins (apoptosis). |
|
|
Term
| Function of Tregs/suppressor |
|
Definition
| Tregs/suppressor cells down-regulate the immune response at the end of an infection |
|
|
Term
| 3 proteins expressed by activated T cell and their functions |
|
Definition
| Enzymes, adapter proteins, and transcription factors are invovled in proliferation, differentiation, and effector functions. |
|
|
Term
| Sequence of activation of T-cell |
|
Definition
| (1) Formation of immunological synapse (TCR/MHC/CD4/CD8, CD28/B7, etc) (2) Activation of Lck on cytoplasmic tail of co-receptors (3) Lck phosphorylates tyrosine residues on tails (ITAMS) (4) Phosphorylated ITAMS is the docking site for Zap-70 (5) Zap-70 is phosphorylated by Lck (6) Zap-70 phosphorylates proteins and enzymes for cell proliferation, differentiation, activation, and protein production |
|
|
Term
| pathways upregulated from T cell activation |
|
Definition
| (1) NFAT (2) NFkB (3) PI3-Akt (4) MapK/ERK/JNK/AP-1. These pathways stimulate production of transcription factors (NFAT, NFkB, AP-1) that migrate to the nucleus and facilitate transcription of cytokines such as IL-2 and cytokine receptors, induction of cell cycle, and production of effector molecules such as CD40 ligand, to upregulate the immune response. |
|
|
Term
| Activation and clonal expansion of lymphocytes |
|
Definition
| occurs within 1-2 days; antigen-specific clones (armies) expand 100,000 fold during this time, and double every 6 hours. |
|
|
Term
| Cytokines produced by helper T cell subsets |
|
Definition
| Th1 -> IFN gamma; Th2 -> IL-4, 5, 13; Th17 -> IL-17, IL-22 |
|
|
Term
| Biological properties of cytokines produced by CD4 T cells: IL-2 |
|
Definition
| survival, proliferation, differentiation of effector and regulatory T cells |
|
|
Term
| Biological properties of cytokines produced by CD4 T cells: IL-4 |
|
Definition
| B cell isotype switching to IgE |
|
|
Term
| Biological properties of cytokines produced by CD4 T cells: IL-5, 13 |
|
Definition
| activation of eosinophils |
|
|
Term
| Biological properties of cytokines produced by CD4 T cells: IL-17, 22 |
|
Definition
| : recruitment of neutrophils, monocytes |
|
|
Term
| Biological properties of cytokines produced by CD4 T cells: IFN gamma |
|
Definition
| activation of macrophages |
|
|
Term
| Biological properties of cytokines produced by CD4 T cells: TGF-beta |
|
Definition
| : inhibition of T cell activation, differentiation of regulatory T cells |
|
|
Term
| What happens to T cell wilthout proper co-stimulation? |
|
Definition
| Without proper co-stimulation, the T cell fails to respond and undergoes anergy |
|
|
Term
| Cell mediated immunity is: |
|
Definition
| CMI is antigen specific, systemic, has memory for future infections of that pathogen |
|
|
Term
| Major functions of T cells: |
|
Definition
| Activate B cells and cytotoxic T cells, Effector function – cell-mediated immunity, Suppression of immunity at the end of an infection |
|
|
Term
| Phases of T cell responses: |
|
Definition
| (1) Naïve lymphocytes search for the foreign antigen they each recognize (2) Exposure to the antigen + costimulation (3) Cytokine secretion to upregulate T cells, B cells, and macrophages (IFN) (4) Clonal expansion of effector cells (5) Apoptosis of effector cells at the end of infection, retention of memory T cells |
|
|
Term
| Pathogen vs. opportunistic pathogen |
|
Definition
| pathogen: causes disease in immunocompetent individuals; Opportunistic pathogen: causes disease in immunocompromised but not immunocompetent individuals |
|
|
Term
| Modes of pathogen transmission |
|
Definition
| air, airborne fluid droplets, food, water, fomites, close/intimate contact |
|
|
Term
| Which surface is most highly susceptible to pathogen invasion? |
|
Definition
| Mucosal surfaces are the most highly susceptible to invasion by pathogens, so several mechanisms protect the MALT |
|
|
Term
| Migration of naïve and effector lymphocytes relies on these interactions: |
|
Definition
| (1) Naïve T cell/endothelial cell with L-selectin/L-selectin ligand (2) Effector and memory T cell/endothelial cell – E and P selectin; LFA-1 or VLA4/LFA-1 or ICAM-1 |
|
|
Term
| How does the immune system handle viral infections? |
|
Definition
| In viral infections, CMI predominates but antibodies help with opsonization of viruses |
|
|
Term
| how does the body remove mycobacteria? |
|
Definition
| Mycobacteria are intracellular organisms, so the body uses CMI to remove mycobacteria |
|
|
Term
| how does the body remove fungal infections? |
|
Definition
| Fungal infections usually use CMI + humoral immunity + complement |
|
|
Term
| What do phagocytes use to eliminate pathogens? |
|
Definition
| Phagocytic cells use ROS, NO, and proteolytic enzymes to eliminate pathogens |
|
|
Term
| Cytoxic T lymphocytes (CTL) effector functions |
|
Definition
| Perforin, Granzymes, Granulysin: These compounds cause apoptosis by inactivating enzymes involved in DNA repair. This causes DNA laddering, blebbing, and formation of apoptotic bodies. FAS-FAS-ligand pathway of apoptosis is the method used to eliminate lymphocytes at the end of an immune response. CD95 = death receptor |
|
|
Term
|
Definition
| forms aqueous channels in microbe membrane |
|
|
Term
|
Definition
| serine proteases that travel through perforin channels, activate cysteine proteases and caspase cascade to cause pathogen apoptosis |
|
|
Term
|
Definition
| travels through perforin channels, activates apoptosis via cytochrome C. Caspase 3 is one of the main initiators of the caspase cascade. |
|
|
Term
| Mechanisms that pathogens use to evade the immune response: |
|
Definition
| (1) Formation of a carbohydrate capsule (2) Liberation of toxins that impair immunity (3) Intracellular survival (4) Extracellular enzymes (degrade immune molecules) (5) Antigenic shift/drift (6) Polysaccharide capsule (antiphagocytic, resistant to complement – the immune system kills with opsonins and phagocytosis) (7) Toxins (damage mucosa, toxic to neutrophils, or superantigens) |
|
|
Term
|
Definition
| Block fusion of lysosomes with phagocytic vacuole, Interfere with acidification of phagolysosome, Trigger apoptosis and death of phagocytic cell. Ex. Mycobacterium tuberculosis, Listeria monocytogenes, Histoplasma capsulatum, Toxoplasma gondii |
|
|
Term
| Suppression of immune system through formation of cytokine analogs |
|
Definition
| (1) Epstein Barr Virus – produces analog of IL-10, (2) Herpes – Fc and C’ receptors – interfere w/ antibody, C’, (3) Cryptococcus – sheds capsule, interferes w/ inflammation, (4) HIV – infects and kills CD4 T cells |
|
|
Term
|
Definition
| point mutations, minor differences |
|
|
Term
|
Definition
|
|
Term
| Humoral immune system characteristics |
|
Definition
| Humoral immune system is antigen-specific, has memory, and includes a change in baseline function (post-infectious antibody titers are elevated for years/decades) |
|
|
Term
| How do B cell antibodies work |
|
Definition
| Antigens have thousands of antigenic epitopes on their surfaces; a clone of B cells makes specific antibodies against many of these antigens in an immune response |
|
|
Term
|
Definition
| protein, highly folded, unevenly charged, must be of sufficient size (Significant with vaccines) |
|
|
Term
| Membrane bound antibodies |
|
Definition
|
|
Term
|
Definition
| IgG, IgA-dimer, IgM-pentomer, IgE-allergy |
|
|
Term
|
Definition
| 2 identical light chains (either kappa or lambda), 2 identical heavy chains joined by disulfide bonds; the N-terminal ends of each chain are highly variable, and are the antigen binding sites (determined in the bone marrow); the C-terminal ends are the constant ends that determine the effector function (isotype class) of the antibody |
|
|
Term
|
Definition
| Opsonin, complement activator, neutralizer |
|
|
Term
| Characteristics of a good antigen |
|
Definition
| (1) Highly folded (lots of anatomic nooks and crannies) (2) Unevenly charged (complementary charges typically necessary) (3) Size qualifications (those less than 1000 daltons are usually haptens) (4) Majority are protein |
|
|
Term
| Sequence of antibody formation |
|
Definition
| (1) Rough draft of BCR is made randomly by allelic exclusion in the bone marrow, (2) Immature B cell travels to the secondary lymphoid organ and awaits antigen, (3) After antigen binding, somatic hypermutation of variable regions in successive generations of B cells makes better antigen fit or worse fit (if it’s worse, it undergoes apoptosis), (4) After somatic hypermutation/affinity maturation is complete, isotype switching occurs |
|
|
Term
| Isotypes of antibodies and their functions in humoral immunity |
|
Definition
| (1) IgG: most common antibody, monomer, 75% of serum Ab; (2) IgM: early Ab, pentamer on surface of B cells, 10% of serum Ab; (3) IgA: present at mucosal surfaces, dimer, 15% of serum Ab. Also important in neonatal passive immunity; (4) IgD: present as bound on naïve B cells, < 1% of serum Ab (because they’re all on B cells…); (5) IgE: monomer, bound to basophils and mast cells, <1% of serum Ab. Important in type I (immediate) hypersensitivity (binds allergens). |
|
|
Term
|
Definition
| neutralization, opsonins, complement fixers |
|
|
Term
| how do antibodies activate NK cells |
|
Definition
|
|
Term
| Which antibodies are the best at activating complement? |
|
Definition
|
|
Term
| Which antigen is found in early infection |
|
Definition
|
|
Term
| Which antigen is most common in established infection? |
|
Definition
|
|
Term
| Which antigen is most commonly found in the blood stream? |
|
Definition
|
|
Term
| What is the function of IgE? |
|
Definition
| IgE binds to a quiescent mast cell then awaits antigen binding to its Fab region, and causes mast cell degranulation and manifestation of allergic symptoms (runny nose, sneezing, coughing, etc) |
|
|
Term
| How do we produce such a large # of antibodies, with our genome being so small? |
|
Definition
| We need random generation of variable regions followed by somatic hypermutation to produce a nearly infinite variety of antibodies to recognize foreign antigens. The variable region of an antibody becomes more specific for its antigen between the time of initial BCR formation in the bone marrow and after somatic hypermutation has been completed. |
|
|
Term
|
Definition
| process by which only one allele of a gene is expressed while the other allele is silenced, so all Ag receptors on a lymphocyte will have the same amino acid sequence in the variable domain of the heavy chain |
|
|
Term
|
Definition
| B cells produce antibodies with increased affinity for antigen during the course of an immune response. With repeated exposures to the same antigen, a host will produce antibodies of successively greater affinities – this happens by somatic hypermutation and clonal selection. |
|
|
Term
|
Definition
| Heavy chain class (there are 5) |
|
|
Term
| The ways that we can achieve antibody diversity: |
|
Definition
| (1) Combatorial diversity during VDJ choosing; (2) Junctional diversity due to imprecise joining of the VDJ segments by RAG; (3) Somatic hypermutation; (4) Random assortment of heavy and light chains |
|
|
Term
| 5 cardinal signs of acute inflammation |
|
Definition
| Pain, swelling, heat, redness, loss of function |
|
|
Term
|
Definition
| pathologic condition where there is persistent active inflammation against a substance that is difficult for the immune system to eliminate; usually characterized by macrophages and lymphocytes, but can also include eosinophils and other cells if there is a persistent allergic or parasitic inflammation. Poison ivy is one example of chronic inflammation. |
|
|
Term
|
Definition
| complex biological response of vascular tissues against harmful stimuli such as pathogens, damaged cells, and irritants. The main purposes of acute inflammation are to stop bleeding, clean up dead cells and pathogens, and promote wound healing. |
|
|
Term
| Four major plasma enzyme systems |
|
Definition
| complement, coagulation, fibrinolytic, kinin |
|
|
Term
|
Definition
| MAC, opsonins, chemotaxins |
|
|
Term
|
Definition
| clotting/hemostasis – produce fibrin strands from soluble fibrinogen |
|
|
Term
|
Definition
| breaks down clots, makes FDPs |
|
|
Term
|
Definition
| mediates changes in vasculature, blood pressure, and pain |
|
|
Term
| Differentiating acute from chronic inflammation with a CBC |
|
Definition
| (1) Acute inflammation involves leukocytosis (esp. neutrophilia) and a left shift (increased band neutrophils); (2) Chronic inflammation involves mature neutrophilia and monocytosis; (3) Stress leukogram involves mature neutrophilia, lymphopenia, eosinopenia (corticosteroid response) |
|
|
Term
|
Definition
| Corticosteroids make neutrophils more sticky, so there’s not more production of them, they’re just trapped in the blood and can’t get out. The lymphocytes and eosinophils tend to stick more in the secondary lymphoid tissues. This is why with chronic stress, you get immune depression. |
|
|
Term
| Gram positive immune response |
|
Definition
| Gram positive immune response involves antibodies against teichoic acid binding to the bacterial cell wall. The antibody becomes an opsonin, and the phagocyte phagocytoses the flagged bacterium. |
|
|
Term
| Gram negative immune response |
|
Definition
| Gram negative bacterial cells have lipopolysaccharide or endotoxin in their cell walls. Endotoxin activates the complement cascade, and the bacterium undergoes complement-mediated lysis (MAC). |
|
|
Term
| Reasons antibodies bind extracellular toxins |
|
Definition
| (1) neutralization of the microbes (by preventing the microbes to infect host cells), (2) inhibition of the spread of microbes/toxins to adjacent uninfected cells, (3) to block binding of toxins to cells inhibiting their pathologic effects. |
|
|
Term
|
Definition
| The phagocyte uses Fc receptor/Fc binding to facilitate immune complex phagocytosis |
|
|
Term
| which system plays a rolein combating viral infections? |
|
Definition
| The humoral immune system plays a role in combating viral infections – at times the virus is extracellular and can be bound by antibody; evidence – vaccination against viruses predominantly upregulates humoral immunity |
|
|
Term
| How are fungal and parasitic infections treated? |
|
Definition
| Fungi and parasites are more difficult for the immune system to combat because they are larger and more complex. Because of this, we often need to administer antifungals/antiparasitics to affected patients; also, these infections are often opportunistic, so the patient’s immune system may be compromised. |
|
|
Term
| Mechanisms that pathogens use to evade immune response: |
|
Definition
| Sugar capsule (polysaccharide capsule); Toxins; Antigenic variation; Intracellular survival; Suppression of immune system; Extracellular enzymes – degrade immune molecules |
|
|
Term
| Objective of immunization |
|
Definition
| to provide long-lasting protection against an infectious agent |
|
|
Term
|
Definition
| administration of a vaccine that elicits protective immune response |
|
|
Term
|
Definition
| administration of antibodies or lymphocytes which provide protection to the recipient host |
|
|
Term
| Major functions of the mucosal immune system: |
|
Definition
| Protect mucous membrane against infection; Prevent uptake of pathogenic antigens; Moderate the immune response against pathogenic foreign material |
|
|
Term
| Why is the mucosa fragile? |
|
Definition
| The mucosa is very fragile because the single cuboidal/columnar epithelium is exposed to many mechanical/thermal/chemical/infectious substances on a daily basis |
|
|
Term
| Mechanisms that the mucosa uses to prevent infectious agents from entering: |
|
Definition
| Mucus; IgA; Gamma-delta T cells; APCs with help of M cells; |
|
|
Term
|
Definition
| (1) Dominant class of antibody in MALT, produced by plasma cells in Peyer’s patches; (2) 3-5 g of IgA secreted daily; (3) Monomer in blood, dimer in MALT; (4) Naïve B cells in the PP undergo somatic hypermutation, then class switching to IgA under control of TGF-beta; (5) IgA actively transported across epithelia, binds to and neutralizes microbes in lumen of mucosal organs – preventing colonization and infection; (6) Transportation/endocytosis to luminal surfaces occurs by Ab binding to a special Fc receptor produced by epithelium |
|
|
Term
| Antigen presenting cells with the help of M cells |
|
Definition
| M cells (microfold cells): cells found in the follicle-associated epithelium of the Peyer’s patch; help facilitate antigen presentation, but can also be taken advantage of and used as a portal for entry – transport organisms/particles from gut lumen to immune cells against the epithelial barrier; take up antigen from SI lumen via endocytosis/phagocytosis and deliver it to APCs and lymphocytes (esp. T cells) via transcytosis |
|
|
Term
| Peripheral tolerance to food |
|
Definition
| the mucosal immune system has learned to allow food peptides across for absorption without immune response, but does respond to pathogenic foreign antigens that try to invade |
|
|
Term
|
Definition
| Commensal organisms basically take up space, not giving other organisms a place to grow/reduce pathogenic adherence. Also, commensal bacteria produce vitamin K and short-chain fatty acids. When broad-spectrum antibiotics wipe them out along with pathogens, it allows for other pathogens to invade that space. This can lead to mucosal injury and bloody diarrhea. |
|
|
Term
| Neonates acquire maternal antibodies 2 ways, both of which rely on neonatal Fc receptor (FcRn). |
|
Definition
| (1) IgG binds to FcR in placenta, and is transported to fetal circulation. Only IgG can be transferred during pregnancy, and it is the predominant Ab type transferred through milk. (2) After birth, neonates ingest maternal antibodies (IgG and IgA) in the mother’s milk. FcR in intestinal epithelium carry mom’s antibodies across the gut epithelium and into the baby’s bloodstream. |
|
|
Term
| Roles of artificial passive immunity |
|
Definition
| Toxin neutralization (Botulinum toxin, tetanus toxin, snake venom); Virus neutralization (Rabies); Bacterial neutralization; Treatment of autoimmunity |
|
|
Term
| How are vaccines administered |
|
Definition
| parentally, orally, intranasally |
|
|
Term
| Precautions for proper vaccine administration |
|
Definition
| Whole community should participate; give to youngest age that CAN get disease; give to those that CAN mount an immune response to the vaccine; be aware of allergies to additives, adjuvants; caution- women of childbearing age |
|
|
Term
|
Definition
| pharmacological or immunological agents that modify the effect of vaccines, while having few if any effects when given by themselves. |
|
|
Term
| How do adjuvant accelerate, prolong, enhance immune response to a vaccine? |
|
Definition
| (1) Helping to translocate antigens to lymph nodes; (2) Prolong longevity of antigens (prevent degradation); (3) Cause local reaction (irritation) at the injection site; (4) Increase release of inflammatory cytokines; (5) Upregulate innate immunity; (6) Can be inorganic (Al salt), organic (oil based), or experimental |
|
|
Term
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Definition
| 1. elderly (with reduced immune response); 2. stress (malnutrition, parasitism, etc); 3. immune compromised patients; 4. presence of maternal Ab (will inactivate the vaccine); 5. expired, improper storage of modified live vaccines; 6. antigenic drift/antigenic shift (ex. Flu virus); 7. improper vaccine administration; 8. the individual is already incubating the disease |
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Term
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Definition
| 1. Inclusion of thimerosal (preservative in influenza and DTP vaccine) that metabolizes into ethylmercury; 2. possible link between MMR and autism; Overdoing vaccines- children get >21 vaccinations before KG; 4. bioterrorism; 5. recalls; 6. ethics |
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Term
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Definition
| Modified live; killed; toxoids; subunit; conjugate; recombinant vector; DNA vaccines |
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Term
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Definition
| Antigen still alive but has lost ability to cause disease (cultured to disable virulence). Advantages: strong, long lasting immunity with fewer doses; adjuvants not necessary; less chance of allergic reaction; quickly stimulate non-specific, antiviral protection via interferon production. Disadvantage: can become virulent again |
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Term
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Definition
| Advantages: more stable in storage, unlikely to contain a contaminating pathogen, unlikely to revert to a virulent strain, may be used in pregnant patients. Disadvantage: often need 2 doses to build up effective immunity – anamnestic response: renewed rapid production of an antibody on the second (or subsequent) encounter with the same antigen. Examples of killed vaccines: flu, cholera, bubonic plague, hep A |
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Term
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Definition
| Inactivated toxic compounds from organisms where the toxin, not the organism itself, causes disease (ex: tetanus, diphtheria) |
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Term
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Definition
| These are made by administering just an immunogenic fragment of a pathogenic organism to create an immune response |
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Term
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Definition
| Certain bacteria have polysaccharide outer coats that are poorly immunogenic. By linking these outer coats to proteins, the immune system can be lead to recognize the polysaccharide as if it were a protein antigen |
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Term
| recombinant vector vaccine |
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Definition
| Experimental; combine non-virulent virus with gene that codes for immune protective protein. So immunity against the virus is encoded inside its own DNA |
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Term
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Definition
| Experimental; DNA of virus or bacteria inserted into human/animal cells. Gene expressed, immune system recognizes foreign Ag. Memory cells are produced that will quickly target that pathogen in future infections |
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Term
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Definition
| branch of pharmacology concerned with the application of immunological techniques and theory to the study of the effects of drugs, esp. on the immune system. Uses: infectious disease, cancer, autoimmune disease |
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Term
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Definition
| Cancer immunotherapy – stimulate immune system to ID, reject, and destroy tumors in the body. Dendritic cell-based immunotherapy – uses DC to activate a cytotoxic response against an antigen (harvested DC pulced with antigen or transfected with a viral vector then returned to patient to increase CMI). T cell based adoptive immunotherapy – T cells harvested from patient, treated with IL-2, and given back to patient in more stimulated form |
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Term
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Definition
| reduced activation/efficacy of the immune system. Application: prevent rejection of organ transplant, treat autoimmune disease, selectively kill cancer cells |
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Term
| Serum proetin electrophoresis |
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Definition
| Serum protein electrophoresis – to look for antibody response to disease. 1st peak: albumin (negative acute phase protein). 2nd peak: acute phase proteins. 3rd peak: IgM (early humoral immune response to infection). 4th peak: IgG (wide-polyclonal-infection: narrow-monoclonal-cancer) |
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Term
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Definition
| to detect antigens on RBC |
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Term
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Definition
| to detect soluble antigens (makes ag-ab immune complexes) |
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Term
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Definition
| assay that sandwiches antigen (or antibody) between 2 antibodies |
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Term
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Definition
| to detect antigens in a slice of tissue |
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Term
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Definition
| separate proteins by size/charge, then expose them to antibodies against one of the proteins; where the ag-ab meet there is a line |
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Term
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Definition
| separate proteins by size and stain to quantify protein |
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Term
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Definition
| separate proteins on a column of beads |
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Term
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Definition
| detect nucleic acid antigens |
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Term
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Definition
| identifies antigens on a microbe that would be most immunogenic; used to choose antigens to be put in vaccines |
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Term
| How can you test how patient is responding to disease? |
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Definition
| isolate specific populations of cells in blood: Neutrophils – production of ROS, phagocytosis; Lymphocytes – proliferation, production of cytokines; Macrophages – phagocytosis, production of cytokines. |
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Term
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Definition
| Tolerance is a state of unresponsiveness to an antigen that is induced by exposure to that antigen |
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Term
| 3 responses of immune cells with antigen exposure |
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Definition
| Proliferation and differentiation and activation; No response (ignore) or anergy (shut down); Undergo apoptosis |
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Term
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Definition
| Central tolerance: tolerance only to self-antigens that are present in primary lymphoid organs. Peripheral tolerance: tolerance to other self-antigens that are not present in thymus or bone marrow must be induced in the periphery. |
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Term
| Central tolerance to self-antigens |
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Definition
| 1. immature lymphocytes that react to self are eliminated; 2. B cells change their specificity (receptor editing); 3. some T cells become Tregs. |
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Term
| Peripheral tolerance to self-antigens |
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Definition
| mature lymphocytes that react to self are eliminated |
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Term
| What if the immune system becomes intolerant of self? |
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Definition
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Term
| What if the immune system is tolerant of pathogens? |
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Definition
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Term
| What if the immune system is intolerant of food proteins? |
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Definition
| food allergies may result |
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Term
| What if the immune system is intolerant of allergens? |
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Definition
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Term
| How can CD4 T cells promote tolerance? |
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Definition
| Lack of costimulatory molecules; Produce CTLA-4 to bind to B7 (instead of CD28) – reverse effect on macrophage and shuts down helper T cell too; Produce inhibitory cytokines like IL-10, TGF-beta; Commit apoptosis. |
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